Ischaemic cardiomyopathy (IC) predominantly arises from prolonged deprivation of oxygen in the coronary arteries, resulting in compromised cardiac contractility or relaxation. This study investigates the role of disulfidptosis-associated genes (DiGs) in IC. Through the analysis of datasets GSE5406 and GSE57338, we explored the association between DiGs and immune characteristics to identify crucial genes contributing to IC development. The support vector machine model emerged as the most effective, identifying key genes such as MYH9, NUBPL, MYL6, MYH10 and NCKAP1. Validation with independent datasets GSE57345, GSE48166 and single-cell GSE145154 further supported these findings, demonstrating high predictive accuracy. Experimental validation in an IC mouse model, using Western blot, immunohistochemistry and RT-qPCR, confirmed the altered expression of these core genes in myocardial ischaemic regions. This research not only elucidates the significance of DiGs in IC but also underscores the diagnostic potential of identified core genes.
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http://dx.doi.org/10.1111/jcmm.70475 | DOI Listing |
Cureus
February 2025
Internal Medicine, University of Florida College of Medicine, Gainesville, USA.
Lyme disease (LD), caused by , is a tick-borne illness that can lead to Lyme carditis, which most commonly presents as a high-degree atrioventricular (AV) block. While conduction abnormalities are well-documented, LD has also been implicated in non-ischemic cardiomyopathy, though this manifestation remains rare and under-recognized. We present the case of a 57-year-old female with newly diagnosed heart failure with reduced ejection fraction (HFrEF) and first-degree AV block, who initially presented with nausea, dizziness, fatigue, and gastrointestinal symptoms.
View Article and Find Full Text PDFJ Cell Mol Med
March 2025
Department of Cardiology, The Fourth Affiliated Hospital of Soochow University, Suzhou Dushu Lake Hospital, Medical Center of Soochow University, Suzhou, China.
Ischaemic cardiomyopathy (IC) predominantly arises from prolonged deprivation of oxygen in the coronary arteries, resulting in compromised cardiac contractility or relaxation. This study investigates the role of disulfidptosis-associated genes (DiGs) in IC. Through the analysis of datasets GSE5406 and GSE57338, we explored the association between DiGs and immune characteristics to identify crucial genes contributing to IC development.
View Article and Find Full Text PDFHereditas
March 2025
Department of Cardiology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.
Background: Acute myocardial infarction (AMI) is the primary cause of cardiac mortality worldwide. However, myocardial ischemia-reperfusion injury (MIRI) following reperfusion therapy is common in AMI, causing myocardial damage and affecting the patient's prognosis. Presently, there are no effective treatments available for MIRI.
View Article and Find Full Text PDFSheng Li Xue Bao
February 2025
Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China.
Cardiovascular disease remains the leading cause of death in China, with its morbidity and mortality continue to rise. Ferroptosis, a unique form of iron-dependent cell death, plays a major role in many heart diseases. The classical mechanisms of ferroptosis include iron metabolism disorder, oxidative antioxidant imbalance and lipid peroxidation.
View Article and Find Full Text PDFEur J Hum Genet
March 2025
Department of Clinical Genetics and Genomics, Sahlgrenska University Hospital, Gothenburg, Sweden.
Pathogenic variants in the EMD gene cause X-linked Emery-Dreifuss muscular dystrophy type 1 (EDMD1), typically presenting with joint contractures and skeletal muscle atrophy, followed by atrial arrhythmias, cardiac conduction defects, and atrial dilatation. Although an association with isolated dilated cardiomyopathy (DCM) has been suggested, evidence is currently insufficient to verify the gene-disease association. We investigated the causality of a missense variant, c.
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